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Last 50 Pulmonary Postings

(Click on title to be directed to posting, most recent listed first, CME offerings in Bold)

Tip of the Iceberg: 18F-FDG PET/CT Diagnoses Extensively Disseminated 
   Coccidioidomycosis with Cutaneous Lesions
July 2017 Pulmonary Case of the Month
Correlation between the Severity of Chronic Inflammatory Respiratory
   Disorders and the Frequency of Venous Thromboembolism: Meta-Analysis
June 2017 Pulmonary Case of the Month
May 2017 Pulmonary Case of the Month
April 2017 Pulmonary Case of the Month
March 2017 Pulmonary Case of the Month
February 2017 Pulmonary Case of the Month
January 2017 Pulmonary Case of the Month
December 2016 Pulmonary Case of the Month
Inhaler Device Preferences in Older Adults with Chronic Lung Disease
November 2016 Pulmonary Case of the Month
Tobacco Company Campaign Contributions and Congressional Support
   of the Cigar Bill
October 2016 Pulmonary Case of the Month
September 2016 Pulmonary Case of the Month
August 2016 Pulmonary Case of the Month
July 2016 Pulmonary Case of the Month
June 2016 Pulmonary Case of the Month
May 2016 Pulmonary Case of the Month
April 2016 Pulmonary Case of the Month
Pulmonary Embolism and Pulmonary Hypertension in the Setting of
   Negative Computed Tomography
March 2016 Pulmonary Case of the Month
February 2016 Pulmonary Case of the Month
January 2016 Pulmonary Case of the Month
Interval Development of Multiple Sub-Segmental Pulmonary Embolism in
   Mycoplasma Pneumoniae Bronchiolitis and Pneumonia
December 2015 Pulmonary Case of the Month
November 2015 Pulmonary Case of the Month
Why Chronic Constipation May be Harmful to Your Lungs
Traumatic Hemoptysis Complicating Pulmonary Amyloidosis
Staphylococcus aureus Sternal Osteomyelitis: a Rare Cause of Chest Pain
Safety and Complications of Bronchoscopy in an Adult Intensive Care Unit
October 2015 Pulmonary Case of the Month: I've Heard of Katy
Pulmonary Hantavirus Syndrome: Case Report and Brief Review
September 2015 Pulmonary Case of the Month: Holy Smoke
August 2015 Pulmonary Case of the Month: Holy Sheep
Reducing Readmissions after a COPD Exacerbation: A Brief Review
July 2015 Pulmonary Case of the Month: A Crazy Case
June 2015 Pulmonary Case of the Month: Collapse of the Left Upper
Lung Herniation: An Unusual Cause of Chest Pain
Valley Fever (Coccidioidomycosis): Tutorial for Primary Care Professionals
Common Mistakes in Managing Pulmonary Coccidioidomycosis
May 2015 Pulmonary Case of the Month: Pneumonia with a Rash
April 2015 Pulmonary Case of the Month: Get Down
March 2015 Pulmonary Case of the Month: Sticks and Stones May
   Break My Bronchi
Systemic Lupus Erythematosus Presenting As Cryptogenic Organizing 
   Pneumonia: Case Report
February 2015 Pulmonary Case of the Month: Severe Asthma
January 2015 Pulmonary Case of the Month: More Red Wine, Every


For complete pulmonary listings click here.

The Southwest Journal of Pulmonary and Critical Care publishes articles broadly related to pulmonary medicine including thoracic surgery, transplantation, airways disease, pediatric pulmonology, anesthesiolgy, pharmacology, nursing  and more. Manuscripts may be either basic or clinical original investigations or review articles. Potential authors of review articles are encouraged to contact the editors before submission, however, unsolicited review articles will be considered.



Congenital Bronchial Atresia: A Case Report with Radiographic and Pathologic Correlation

Lewis J. Wesselius, MD1

John R. Muhm, MD2

Henry D. Tazelaar, MD3

Departments of Pulmonary Medicine1, Radiology2, and Laboratory Medicine- Pathology3, Mayo Clinic Arizona, 13400 East Shea Boulevard, Scottsdale, AZ 85259

Reference as: Wesselius LJ, Muhm JR, Tazelaar HD. Congenital bronchial atresia: a case report with radiographic and pathologic correlation. Southwest J Pulm Crit Care 2011;3:64-9. (Click here for a PDF version)


Bronchial atresia is a rare congenital disorder characterized by localized atresia or stenosis of a segmental bronchus.  Imaging features typically include mucus impaction in distal airways associated with regional lung hyperlucency. Pathologic features of bronchial atresia have been rarely been reported.  This case demonstrates CT features of this disorder as well as the unusual finding of increased lung uptake of 18F-fluorodeoxyglucose on PET scan.  This finding led to a surgical lung biopsy to exclude infectious or neoplastic disorders.  This case provides radiologic-pathologic correlation in a patient with congenital bronchial atresia and demonstrates that localized, mildly increased uptake on PET scan be associated bronchial atresia.

Case Presentation

A 35-year-old woman was referred for evaluation of an abnormal thoracic CT scan.     An abnormality was noted on a routine chest radiograph 2 years previously, and thoracic CT reportedly showed an “infiltrate” in the right upper lobe.  Bronchoscopy with bronchoalveolar lavage performed 1 year previously was reportedly negative.  The patient was asymptomatic and denied any cough, fever or shortness of breath.  On physical examination the patient was afebrile and the chest examination was within normal limits.  She had a normal complete blood count and serologic studies for coccidioidomycosis were negative.  A recent chest radiograph (Figure 1) and thoracic CT (Figure 2) performed at the referring medical center demonstrated abnormalities in the right upper lobe, without clear visualization of the posterior segment right upper lobe bronchus. Repeat bronchoscopy was performed which and reportedly demonstrated a patent right upper lobe posterior segmental bronchial orifice, although limited visualization into the airway was noted.  Microbiologic studies and cytologic examination of the bronchoalveolar lavage fluid were negative.

Figure 1:   Chest radiograph performed one month prior to presentation shows small nodular opacities of indeterminate etiology in the right upper lung.

Figure 2:  Thoracic CT shows atresia of the central portion of the right upper lobe posterior segment bronchus (arrow).  In the right upper lobe posterior segment, peripheral to the atretic bronchus, numerous irregular opacities resulting from dysplastic bronchi filled with mucus are noted.  The hypoattenuating areas in the right upper lobe posterior segment represent hypoperfused secondary pulmonary lobules resulting from the obstructed, dysplastic bronchioles.

Subsequent Clinical Course

Subsequent 18F-fluorodeoxyglucose positron emission tomography (FDG- PET, Figure 3) scan performed at the outside medical center showed hypermetabolism within the right upper lobe, with a standard uptake value (SUV) of 2.9.

Figure 3: Image from Coronal FDG-PET shows areas of mild-to-moderate increased uptake (SUV 2.2) in the posteromedial aspect of the right upper lobe.

The finding of elevated FDG uptake on PET scan, as well as an increase in the extent of CT abnormalities, raised clinical concern for an undiagnosed infectious process or low-grade malignancy. The patient subsequently underwent a thoracoscopic lung biopsy at the outside institution to exclude those possibilities.

Further radiology review of the lung CT scan was concurrently requested by the referring physician and the radiographic features of bronchial atresia involving the posterior segment of the right upper lobe were noted.  There was a dysplastic bronchus supplying the posterior segment of the right upper lobe, filled with mucus, and associated with evidence of hypoperfusion of that segment.  Review of the tissue obtained at lung biopsy (Figure 4) demonstrated mucus impaction in small airways, consistent with changes secondary to bronchial atresia.  There was no evidence of active infection or a neoplastic process.

Figure 4: VATS biopsy specimen obtained from the right upper lobe.  The biopsy shows a chronic bronchiolitis (a) with lymphoid hyperplasia and germinal centers ( There is also prominent bronchiolectasis (c) with mucostasis in the airway lumen and extending into the surrounding lung (d).


Bronchial atresia is an uncommon congenital tracheobronchial abnormality first described in 1953 and is characterized by stenosis of a segmental airway (1). The abnormality generally involves a single segment, although cases with mult- isegment involvement have been reported (2).  The apical-posterior segment of the left upper lobe is most frequently involved, followed by segments within the right upper, middle and lower lobes (3,4).  This abnormality is frequently asymptomatic and is incidentally detected on chest radiography in 58% of cases (2). Patients may present, often in early adulthood, with symptoms of recurrent infections (21%), dyspnea (14%) and cough (6%). Cases associated with spontaneous pneumothorax have been reported (5).

The diagnosis of congenital bronchial atresia can generally be made from thoracic CT findings alone. Characteristic imaging findings include mucus impaction in dilated airways distal to the area of stenosis (6), typically associated with  regional pulmonary parenchymal hyperlucency due to hypoperfusion, representing mosaic perfusion, resulting from obstructed dysplastic bronchi.

Bronchoscopy can be helpful to exclude competing diagnostic considerations and to exclude infectious processes.  In some patients, segmental airway atresia or an obvious narrowing may be directly observed at bronchoscopy.  However, the area of stenosis is not always visible at bronchoscopy (7). In our patient, the bronchoscopy did not clearly identify an area of segmental narrowing, although that finding was suggested by the CT scan (Figure 2).

FDG-PET (Figure 3), performed to evaluate for a possible undiagnosed infectious or malignant process, showed increased uptake in the areas of radiographic abnormality.      However, subsequent VATS biopsy of the right upper lobe was negative for any infectious or neoplastic process.  Increased uptake pulmonary parenchymal on FDG-PET scan is commonly seen in lung neoplasms and infections, but has also been reported in non-infectious inflammatory lung conditions, including sarcoidosis and idiopathic pulmonary fibrosis (8,9).  There are prior case reports of localized pulmonary parenchymal uptake on FDG-PET scans performed in patients with benign airway disorders, including acute bronchitis and allergic bronchopulmonary aspergillosis (10,11).  The finding of increased uptake on FDG-PET scan has not previously been reported in patients with congenital bronchial atresia.  The specific reason for the localized uptake in the pulmonary parenchyma distal to the atretic bronchus in our patient is not certain. It is possible that local inflammation associated with mucostasis contributed to this finding as there was some evidence of interstitial inflammation noted on the surgical lung biopsy.

The lung biopsy obtained in this patient showed findings consistent with bronchial atresia including mucostasis in airways. The finding of mucostasis correlates with the CT findings of mucus impaction in dilated airways.  Review of the literature indicated only one prior report of pathologic findings in patients with bronchial atresia (12). The findings in our case- respiratory bronchioles plugged with mucus- are consistent with those previously reported. Dilation of surrounding alveoli without evidence of destruction has also been previously reported, consistent with air-trapping.


Congenital bronchial atresia is an uncommon disorder that can present with a specific pattern on thoracic CT performed on asymptomatic patients or patients with respiratory symptoms of recurrent infections, dyspnea and cough. Bronchoscopy can be helpful to exclude other diagnostic considerations and may demonstrate evidence of segmental bronchial stenosis, although the area of stenosis may not be evident in all cases. Our patient presented with the unusual finding of mildly increased, localized uptake of FDG-PET scan, a finding previously unreported.  Lung biopsy confirmed pathologic features consistent with bronchial atresia, including airway dilatation and terminal bronchial mucus impaction.


  1. Ramsey BH, Byron FX.  Mucocele, congenital bronchiectasis and bronchogenic cyst. J. Thoracic Surg 1953;26:21-30.
  2. Jederlinic PJ, Sicilian L, Baigelman W, et al.  Congenital bronchial atresia – a report of 4 cases and a review of the literature.  Medicine 1986;65:73-83.
  3. Meng RL, Jensik RJ, Faher LP, Matthew GP, Kittle CF.  Bronchial atresia, Ann Thoracic Surg 1978;25:184-192.
  4. Muller NL, Fraser RS, Colman N, Pare P.  Developmental and hereditary lung disease.  In: Radiologic diagnosis of diseases of the chest.  Philadelphia, PA: Saunders; 2001: 125-128.
  5. Berkman N, Bar-Ziv J, Breuer R.  Recurrent spontaneous pneumothorax associated with bronchial atresia.  Resp Med 1996;90:307-309.
  6. Matsushima H, Takoyanagi N, Satoh M, et al.  Congenital bronchial atresia: radiologic findings in nine patients.  J Comp Assist Tomog  2002;26:860-864.
  7. Ward S. Morcos SK. Congenital bronchial atresia – presentation of three cases and a pictoral review.  Clin Radiol 1999;54:144-148.
  8. Brudin LH, Balind SO, Rhodes CG, et al.  Fluorine-18 deoxyglucose uptake in sarcoidosis measured with positron emission tomography.  Eur J Nucl Med 1994;21:297-305.
  9. Groves Am, Win T, Screaton NJ, et al.  Idiopathic pulmonary fibrosis and diffuse parenchymal lung disease: implications from initial experience with18F-FDG PET/CT. J Nucl Med 2009;50:538-545.
  10. Kicska G, Zhuang H, Alavi H.  Acute bronchitis imaged with F-18 FDG positron emission tomography.  Clin Nucl Med 2003;28:511-512.
  11. Nakajima H, Sawaguchi H, Hoshi S, Nakajimo S, Tohda Y.  Intense 18F- fluorodeoxyglucose uptake due to allergic bronchopulmonary aspergillosis. Jap J. Allergology 2009;58:1426-32.
  12. Gipson MG, Cummings KW, Hurth KM. Bronchial atresia  Radiographics 2002;29:1531-1535.

Pulmonary Nocardiosis and Empyema in a Patient with Metastatic Neuroendocrine Tumor

Nimesh K. Patel, DO

Linda Snyder, MD

University of Arizona, Department of Medicine. Tucson, Arizona

Reference as: Patel NK, Snyder L. Pulmonary nocardiosis and empyema in a patient with metastatic neuroendocrine tumor. Southwest J Pulm Crit Care 2011;3:28-33. (Click here for a PDF version)


Nocardia is a ubiquitous aerobic gram-positive bacterium that can cause local or disseminated infection. Nocardiosis involves the lung in the majority of cases. Nocardiosis is often an opportunistic infection, but can also affect non-immunocompromised hosts. This case report highlights the presence of empyema due to Nocardia cyriacigeorgica infection, an unusual feature of Nocardia pulmonary involvement. 

Case Presentation

History of Present Illness: A 65 year-old male with a history of metastatic neuroendocrine tumor of the pancreas, was admitted to the hospital with a one-week history of hemoptysis, cough, and dyspnea. He was treated for presumed community acquired pneumonia with moxifloxacin two weeks prior to admission. He was receiving monthly octreotide injections for treatment of the neuroendocrine tumor. The patient had no history of corticosteroid use.  

Physical examination:

Vital signs: Temperature 99.9F, Respirations18, Blood Pressure 104/69, Pulse 96, SaO2 91% on oxygen at 2 liters per minute by nasal cannula

General: The patient was in no acute distress. He was alert and oriented to person, place and time.

HEENT: No significant abnormalities.

Chest: Dullness to percussion, mid-lower right thoracic cavity, with scattered crackles. 

Cardiovascular: regular rate, normal S1 and S2, no murmurs appreciated.  Abdomen: positive bowel sounds, soft, non-tender, non-distended, positive hepatosplenomegaly. 

Extremities: +2 pitting edema bilaterally extending to mid-thigh level

Laboratory and radiographic findings: The peripheral white blood cell count was 8, 000 cell/mm3 with a differential as follows 91% neutrophils/bands, 7% lymphocytes, 1% myelocyte, 1% reactive lymphocyte, hemoglobin was 11 g/dL and the platelet count was normal. The basic metabolic panel revealed blood urea nitrogen of 30 mg/dl and creatinine of 1.5 mg/dl. The hepatic panel was normal except for an elevated alkaline phosphatase of 530 IU/L. Coccidioides IgM and IgG serology performed by immunodiffusion were negative.

The chest radiographs from two weeks prior to admission (Figure 1), admission (Figure 2) and admission computerized tomography of the chest (Figure 3) are shown.  

Figure 1. Chest radiograph two weeks before admission:  Right middle lobe consolidation with volume loss and small right pleural effusion


Figure 2.  Chest radiograph on admission: Increasing patchy opacifications involving the right upper lobe, right middle lobe, and left lower lobe, with cavity formation noted in the left lung. There is right paratracheal lymphadenopathy noted.

Figure 3: Computerized tomography of the chest showing multifocal consolidation with a necrotizing process containing central lucencies. A loculated, moderate sized right anterior pleural effusion with lucencies is compatible with an empyema.

Hospital course:

Our patient was started on broad-spectrum antimicrobial therapy and underwent chest tube drainage of the loculated effusion.  A sputum gram stain revealed 4+ weakly acid-fast branching bacilli, consistent with Nocardia. The gram stain of the pleural fluid showed 3+ polymorphonuclear cells and 3+ gram-positive, branching, weakly acid-fast bacilli, consistent with Nocardia.  The culture from sputum and pleural fluid grew Nocardia cyriacigeorgica

Computerized tomography of the brain showed no intracranial abnormalities. The patient was treated with high dose trimethoprim/sulfamethoxazole, two double strength tablets three times a day with monitoring of sulfamethoxazole levels. The patient clinically improved with antimicrobial treatment and drainage of the empyema. The chest tube was successfully removed and the patient’s symptoms of cough and dyspnea resolved. A chest x-ray showed resolution of the right middle lobe and left lower lobe infiltrative process.

Figure 4.  Chest radiograph post-antimicrobial treatment: Interval resolution of right middle lobe and left lower lobe infiltrative process. Post infectious inflammatory changes are noted in the right middle lobe.


Nocardiosis is an important opportunistic infection caused by aerobic actinomycetes in the genus Nocardia. Nocardia asteroides has been considered the most common species to cause human disease, however classification has become more complex with the use of molecular techniques. Species formerly included in the Nocardia asteroides complex are now considered distinct species.  Nocardia cyriacigeorgica is one of the more common isolates and has been noted to cause pleural disease and empyema.  Nocardia species are found in soil and can become airborne; the most common route of entry for infection is inhalation. Effective cell-mediated immunity of the host is crucial to combating infection with Nocardia species.  Two recent reviews of nocardiosis highlight important clinical features of this disease (1,2). The most common symptoms are fever, cough, pleuritic chest pain and headache. Specific risk factors for Nocardia infection are present in the majority of patients and include corticosteroid treatment and immunosuppression. Additional risk factors include malignancy and chronic lung disease. Of interest to pulmonologists, chronic obstructive pulmonary disease (COPD) was a common underlying condition, representing over 20% of patients with nocardiosis in these reports. Common chest radiographic presentations of pulmonary nocardiosis include consolidation, nodules and cavities. The diagnosis of pulmonary nocardiosis is made from sputum and bronchoalveolar lavage specimens in the majority of patients. In addition, recent reviews document that pleural effusions are present in up to 35% of patients with pulmonary nocardiosis.  In one report, when pleural fluid was sampled, Nocardia was isolated in the majority of patients. Nocardia cyriacigeorgica can cause invasive pulmonary disease and was found to be the predominant species in pulmonary nocardiosis in one review.


Nocardiosis is an important opportunistic pulmonary disease. The diagnosis should be included in the differential diagnosis of pulmonary infiltrates in immunosuppressed populations, including patients after organ transplantation, with advanced HIV infection and those receiving chronic corticosteroid therapy or chemotherapy. Radiographic findings of lung involvement are variable and include single or multiple nodules or cavities, alveolar or interstitial infiltrates, and pleural effusions. This case report highlights the unusual presentation of Nocardia cyriacigeorgica pulmonary infection with extensive cavitary parenchymal disease and concomitant empyema. 


  1. Minero MV, et al. Nocardiosis at the Turn of the Century.  Medicine 2009;88:250-61.
  2. Tomas RM, et al. Pulmonary Nocardiosis: Risk factors and outcomes. Respirology 2007;12:394-400 .
  3. Latef SM, et al. Nocardia cyriacigeorgica empyema in 45-yr-old male with dual granulomatous lung disease. Chest 2008 134:c12001.
  4. Schlaberg R. Nocardia cyriacigeorgica: an emerging pathogen in the United States.  Journal of Clinical Microbiology 2008;46:265-73.
  5. Maraki S. Nocardia cyriacigeorgica pleural empyema in an immunocompromised patient.  Diagnostic Microbiology and Infectious Disease 2006;56:333-5.




Manmadha Rao Talluri, M.D.

Department of General Medicine, Nizam’s Institute of Medical Sciences, Hyderabad, INDIA

Reference as: Talluri MR. Sandstorm in the chest? Southwest J Pulm Crit Care 2011;3:1-4. Click here for a PDF version

Corresponding Author:

Dr.Manmadha Rao Talluri

Associate professor

Department of General Medicine

Senior Pulmonologist

Nizams institute of Medical Sciences,

Panjagutta, Hyderabad, India

Phone – 914023489240





A 32 year old female presented with dry cough and progressive breathlessness of one year duration. There was no history suggestive of collagen vascular disease, lung parenchymal infection or allergic airway disease. Clinical evaluation showed basal fine inspiratory crepitations. Radiographic examination of the chest revealed a black pleura line and lung parenchymal calcification. CT scan of the chest demonstrated nodular calcification of lung parenchyma with a “crazy pavement” pattern, which is suggestive of alveolar calcification. Pulmonary function test showed a severe restrictive defect. On transbronchial lung biopsy calcific spherules suggestive of the alveolar microlithiasis were seen. Diagnosis of pulmonary alveolar microlithiasis was made and symptomatic treatment was given, as there is no specific therapy available. The case illustrates an unusual cause of shortness of breath in a young female with striking radiographic features. 

Case Summary

History and Physical Examination: A 32 year old woman presented with dry cough and progressive exertional shortness of breath of one year duration. There was no history of bronchial asthma, varicella, rheumatic heart disease, recurrent respiratory tract infections, tuberculosis, occupational dust exposure or connective tissue disease. Furthermore there was no family history of similar complaints but family members were unavailable for screening. Clinical examination showed normal vital signs, facial puffiness with acne and no clubbing. Upper respiratory tract examination was normal. Fine end inspiratory crepitations were heard on lung auscultation. No rhonchi or wheezing was heard. The remainder of the physical examination was normal.

Laboratory Evaluation: Complete blood count, urine examination and renal function tests were within normal limits. Calcium and phosphate were normal. A parathyroid hormone level was not performed. Immunological evaluation showed an antinuclear antibody (ANA) of 1:1 and a rheumatoid factor 42 IU/ml (normal < 30 IU/ml). DsDNA, Anti SS-a, SS-b and U1 RNP were all negative.

Radiography: Radiograph of the chest shown multiple high-density pulmonary nodules in both the lung fields involving all zones with increased density noted in the bases, with a sand storm appearance and a black pleura line (Figure 1).

Figure 1 Radiograph of the chest shows multiple high density pulmonary nodules in both lungs involving all zones with increased density in base as compared to apex, with sand storm appearance and bilateral black pleural lines indicated by the white arrows.

CT scan of the chest is shown in Figure 2.

Figure 2. CT scan cross-sectional imaging showing multiple calcific densities in both lungs with thickening and increased density along the fissure and along the mediastinal margin. A black pleural line is noted.

Additional Studies: Pulmonary function test demonstrated a severe restrictive defect. Ultrasound abdomen was normal with no evidence of nephrocalcinosis. Two dimensional echocardiography was normal. Transbronchial biopsy of the lung showed calciphic spherules, which is the hall mark of the pulmonary alveolar microlithiasis (Figure 3).

Figure 3. Transbronchial biopsy showing intra-alveolar calcific spherules (H & E, X 200). Insert shows higher magnification of calcific spherules (H&E, X400).

Genetic studies and level of surfactant A and D were not measured.

Clinical Course: The patient was continued on corticosteroids and theophyllines empirically added for dyspnea. Bisphosphonates or chelating agents were not used. She was advised to undergo lung transplantation; which could not be done due to financial constraints. The patient gradually worsened over 2 years and succumbed due to respiratory failure. Permission for an autopsy was not granted.


Pulmonary alveolar microlithiasis is a rare disease of unknown etiology, characterized by wide spread laminated clacipherites in alveolar spaces. Other causes of diffuse lung calcification include following tuberculosis, varicella, silicosis, and the metastatic calcification seen with hypercalcemia or renal disease (1).

Pulmonary alveolar microlithiasis is usually sporadic, but an autosomal recessive form has been described in Mediterranean countries (1). The disease is characterized by paucity of symptoms despite wide spread involvement of the lung. Usually presenting in the third or fourth decade of life with cough and dyspnea, pulmonary alveolar microlithiasis usually is a progressive disease with an insidious clinical course resulting in respiratory failure (1,2).

Calcium metabolism has been reported as normal in pulmonary alveolar microlithiasis. Changes in the alveolar membrane secretions resulting in greater alkalinity have been hypothesized to play a major role in the pathogenesis of the disease. The change in alkalinity promotes the intra alveolar precipitation of calcium phosphates. Mutations in the SLC34A2 gene in type II pneumocytes that encodes type IIb sodium phosphate co-transporter have been reported (3). Serum surfactant protein A&D are markedly elevated, which can be useful to monitor the disease activity and progression (4).

Radiograph of the chest is characterized by the presence of a “sand storm” appearance and a black line along the pleura. CT scan usually shows bilateral lung parenchymal nodular calcifications and a “crazy paving” pattern, which is not specific for the diagnosis of pulmonary alveolar microlithiasis (5). Crazy paving has a variety of other causes some of which follow: infectious (Pneumocystis), neoplastic (mucinous bronchoalveolar carcinoma), idiopathic (pulmonary alveolar proteinosis, nonspecific interstitial pneumonitis), inhalational (lipoid pneumonia), and sanguineous disorders (pulmonary hemorrhage syndromes). 

Unfortunately, no established treatment is available.  Management with corticosteroids, chelating agents, bisphopshonates and bronchoalveolar lavage have all been disappointing. The only viable option for these patients is the bilateral lung transplantation (1).


Pulmonary alveolar microlithiasis is a rare disorder, which should always be considered in the differential diagnosis of calcific micronodular pulmonary lesions.


1. Tachibana T, Hagiwara K, Johkoh T. Pulmonary alveolar microlithiasis: review and management. Curr Opin Pulm Med 2009;15:486-490.

2. Castellana G, Gentile M, Castellana R, Fiorente P, Lamorgese V. Pulmonary alveolar microlithiasis: clinical features, evolution of the phenotype, and review of the literature. Am J Med Genet 2002;111:220-224.

3. Huqun, Izumi S, Miyazawa H, Ishii K, Uchiyama B, Ishida T, et al. Mutations in the SLC34A2 gene are associated with pulmonary alveolar microlithiasis. Am. J. Respir. Crit. Care Med  2007;175:263-268.

4. Takahashi H, Chiba H, Shiratori M, Tachibana T, Abe S. Elevated serum surfactant protein A and D in pulmonary alveolar microlithiasis. Respirology 2006;11:330-333.

5. Gasparetto EL, Tazoniero P, Escuissato DL, Marchiori E, Frare E Silva RL, Sakamoto D. Pulmonary alveolar microlithiasis presenting with crazy-paving pattern on high resolution CT. Br J Radiol 2004;77:974-976.

This case was presented at the Great Cases session during the American Thoracic Society meeting in Denver, CO on May 15, 2011. A PowerPoint slide presentation was prepared for than session and a link to the slides is below.

Click here for a PowerPoint slide presentation



Roxanne Garciaorr

Richard A. Robbins

Phoenix VA Medical Center, Phoenix, AZ

Reference as: Garciaorr R, Robbins RA. A middle-aged man with a history of renal cell carcinoma. Southwest J Pulm Crit Care 2011;2:79-84. (Click here for PDF version)

Presented at the Arizona Thoracic Society April, 2009 in Scottsdale, AZ and the Great Cases Session at the American Thoracic Society International Conference, May, 2011 in San Diego, CA. 


A 56 year old man was seen with a lung nodule. He had an extensive past medical history including renal cell carcinoma, congestive heart failure, obstructive sleep apnea and a 135 pack-year history of smoking. His physical examination was consistent with congestive heart failure. Sputum cultures for bacteria, fungi and tuberculosis were all negative. A CT scan revealed a spiculated, noncalcified 2.1 mass in the right lower lobe.  PET scan showed the lesion to have a standard uptake value of 1.5. The lesion was followed and after 3 months had enlarged to 6.4 cm. Biopsy was done and consistent with a lung abscess. Conservative therapy resulted in resolution only to have the lesion recur 22 months later with the patient expiring from massive hemoptysis and respiratory failure. This case illustrates the usefulness of doubling time in separating benign from malignant lung lesions.

Case Presentation

History of Present Illness.

A 56 year old man was seen in pulmonary consultation because of a right lower lobe mass discovered incidentally during a CT scan for pulmonary embolism. He was admitted to the Phoenix VA with complaints compatible with congestive heart failure. He had an extensive PMH with multiple myocardial infarctions with stent placements; resultant congestive heart failure; obesity: type 2 diabetes mellitus; obstructive sleep apnea, a 135 pack-year history of smoking; and right renal cell carcinoma found incidentally in 2006 with subsequent right nephrectomy 2 years previously.

Physical Examination

The patient was a tall, obese man who was afebrile.  Bilateral rales were noted about half way up the lung fields bilaterally and 2+ pretibial edema. The remainder of the physical examination was unremarkable.

Laboratory Findings

Urine analysis, complete blood count, and basic metabolic panel had the following abnormalities and pertinent negatives: hemoglobin 11.0 g/dl; hematocrit 31.9%; WBC 8200 cells/microl; creatinine 1.9 mg/dl; BUN 41 mg/dl; glucose 200 mg/dl. Hemoglobin A1C was 8.9% and a brain naturetic peptide was 887 pg/ml. Arterial blood gases were PaO2 82 mm Hg, PaCO2 25 mm Hg and pH 7.44 while breathing room air. Sputum cultures for bacteria, fungi and tuberculosis were negative. Serology testing for Coccidiomycosis was negative.


The admission chest x-ray is shown in Figure 1.


Figure 1. Admission chest X-ray.

A representative slice of the CT scan showing the right lower lobe mass is shown in Figure 2.


Figure 2. Chest CT showing noncalcified, spiculated 2.1 cm nodule in the right lower lobe indicated by the arrow.

A PET scan was performed and the lesion had a standard uptake value of 1.5.

Subsequent Course

Multiple diagnosis including lung cancer, metastatic renal cancer, and infection were considered. The patient was reluctant to undergo biopsy but agreed to an outpatient course of doxycycline and a repeat CT scan 3 months later (Figure 3).


Figure 3. Repeat CT scan done 3 months later showing enlargement of the right lower lobe mass to 6.4 cm indicated by the arrow.

The patient was agreeable to needle biopsy (Figure 4).


Figure 4. Needle aspiration of lung mass showing an absence of malignant cells with acute inflammation compatible with a lung abcess.

Gastroenterology consultation was obtained and esophageal motility and esophogastroduodenoscopy revealed only gastritis.

The patient was followed and a repeat CT scan done 3 months later revealed shrinkage of the lesion (Figure 5).


Figure 5. CT scan done 6 months after biopsy (9 months after original CT scan). The right lower lobe lesion appears smaller at 1.2 cm.

The patient was followed and was asymptomatic until 22 months after initially seen when he presented with hemoptysis and shortness of breath. Repeat CT scan again showed a lesion in the area of the original lesion with cavitation and an air fluid level (figure 6).


Figure 6. CT scan done 22 months after original CT scan showing cavitation and an air fluid level indicated by the arrow.

Bronchoscopy with bronchoalveolar lavage was performed. Cultures for bacteria, fungi and tuberculosis were negative. He subsequently died from massive hemoptysis and respiratory failure.


This case demonstrates the usefulness of doubling time in separating malignant from nonmalignant chest lesions. Between his first and second CT scans this patient’s lesion had enlarged from 2.1 to 6.4 cm over 102 days giving a calculated doubling time of 21 days (1). Lung cancers generally have average doubling times of about 100 days but have been reported to vary between 30 and 500 days. Doubling times of < 30 days usually indicate an infectious process. The lesion was aspirated because of its growth but no organism was identified. However, doubling time may occasionally be difficult to determine when nodules are not spherical or the borders are particularly vague such as in ground glass opacities or semi-solid lesions.

Narrowing the initial cause of this lung lesion was difficult because of the multiple potential causes including lung cancer, infection, pseudotumor and metastatic renal cell carcinoma. PET scans are usually positive in lung cancers. Negative PET scans have been reported with renal cell carcinoma although in the minority of instances (2). PET scans may be variably positive in pulmonary infections (3). However, the low uptake on PET scanning suggested the lesion was not malignant. Furthermore, the rapid growth combined with the low metabolic uptake also suggested the lesion is not malignant because growth of malignant stage I lung cancers and metabolic activity on PET scanning usually correlate (4).

The infectious cause of this patient’s right lower lobe abscess was never identified despite repeated sputum cultures, bronchoscopies and even a needle aspiration biopsy. Despite the negative evaluation for esophageal dysmotility, it seems most likely that aspiration caused with a subsequent anaerobic abscess was the cause of his lesions. Anaerobic organisms can be difficult to culture (5,6). The patient repeatedly denied any difficulty swallowing, water brash, etc.

It is unclear whether the original lesion identified was the same as the subsequent cavity with an air fluid level. Although progressive pneumonia can occur with aspiration, we suspect repeated aspiration as the subsequent cause of his cavity because of the improvement followed by the worsening 22 months after the initial presentation (5). However, prevention of aspiration may be difficult and it is unclear what measures could have been invoked to prevent his eventual demise.


  1. (accessed 3-29-11).
  2. Chang CH, Shiau YC, Shen YY, Kao A, Lin CC, Lee CC. Differentiating solitary pulmonary metastases in patients with renal cell carcinomas by 18F-fluoro-2-deoxyglucose positron emission tomography--a preliminary report. Urol Int 2003;71:306-9.
  3. Bomanji J, Almuhaideb A, Zumla A. Combined PET and X-ray computed tomography imaging in pulmonary infections and inflammation. Curr Opin Pulm Med. 2011;17:197-205.
  4. Tann M, Sandrasegaran K, Winer-Muram HT, Jennings SG, Welling ME, Fletcher JW. Can FDG-PET be used to predict growth of stage I lung cancer? Clin Radiol 2008;63, 856-863.
  5. Dines DE, Titus JL, Sessler AD. Aspiration pneumonitis.  Mayo Clinic Proc 1970;45:347-60.
  6. Bynum LJ, Pierce AK. Pulmonary aspiration of gastric contents. Am Rev Respir Dis 1976;114:1129-36.

This case was presented at the Great Cases session during the American Thoracic Society meeting in San Diego, CA on May 17, 2009. A link to the slides used for that presentation is below.

Click here for a PowerPoint slide presentation



Johnson Samuel MD, FRCP

Balamugesh Thangakunam, MD, DM 

Basildon University Hospital, United Kingdom 

Presented at the Great Cases Session at the American Thoracic Society International Conference, May 16, 2010 in New Orleans, LA.

Reference as: Samuel J, Thangakunam B. A young lady with vanishing lung shadows. Southwest J Pulm Crit Care 2011;2:40-4. (Click here for PDF version)


   A previously well 20-year-old young lady who presented with nonspecific right-sided chest pain was found to have a rounded shadow on chest X-ray. Investigations to rule out malignancy revealed multiple lung masses. Initial blood tests and percutaneous image guided biopsy were inconclusive. Surgical lung biopsy revealed features suggestive of Bronchocentric Granulomatosis. Her lung shadows spontaneously resolved and there was no evidence of symptomatic or radiological recurrence on follow up for five years. Bronchocentric Granulomatosis is a rare condition particularly in non-asthmatic individuals and should be considered in the lesser-known differential diagnosis of benign lung shadows. 

Case Presentation 

History and Examination

   A 20-year-old lady presented to the Emergency department with right-sided pleuritic chest pain after watching a football match in the local pub.  A Chest radiograph showed a 1cm oval opacity in the periphery of the left upper zone. She was treated with a course of antibiotics and a repeat chest radiograph two weeks later showed an increase in the size of the opacity (Fig 1).


Figure 1.  Chest radiograph showing a rounded opacity in left upper zone.

   She was then referred to the respiratory clinic for evaluation. She was a non-smoker with no previous medical history of note. There was no history of recent respiratory infections. Clinical examination including breast examination was entirely normal.


    Haemoglobin was 11.2 gm/dl, white cell count 7.0 x109/L, platelet count 255x109/L and erythrocyte sedimentation rate 22mm/hr. Differential white cell count was normal with absolute eosinophil count 0.1x109/L.  Serum angiotensin converting enzyme was 36 IU/L. Serum compliment levels were normal and tumour markers were negative. Human chorionic gonadotrophin level was not elevated. Rheumatoid factor was 38 IU/ml, autoantibodies and Human Immunodeficiency Virus tests were negative. Mantoux test was non-reactive

   Computed Tomography (CT) showed three opacities, two of which were on the right side (Fig 2).

 Figure 2.  Computerised Tomography scan of chest showing bilateral lung opacities

   A CT guided biopsy showed necrotizing chronic granulomatous inflammation with no evidence of malignancy. There were many eosinophils seen in the biopsy sample (Fig 3).



Figure 3.  Computerised Tomography guided biopsy of the lesion showing necrotizing granulomatous inflammation. The arrowheads indicate necrosis centre of the picture with many eosinophils. The area circled shows a granuloma including a multi-nucleated giant cell indicated by the short arrow. (High power view- formalin fixed, haemotoxylin and eosin staining).

   As the diagnosis was still uncertain and as there was the suspicion of metastatic malignancy of uncertain origin, she underwent a video assisted thoracoscopic biopsy (VATS biopsy). Histopathology of the nodule revealed abundant necrosis, surrounded by a rim of chronically inflamed fibrous tissue with focal areas of discontinuous elastic lamina (Fig 4).

Figure 4.  Video assisted thoracoscopic biopsy showing focal necrotizing granulomatous inflammation. Arrowhead indicated the central necrosis. Short arrow indicated the multi-nucleated giant cell (High power view – formalin fixed, haemotoxylin and eosin staining).

   Mycobacterial and fungal cultures were negative. There were no features of vasculitis or malignancy.  Based on the histopathology and the clinical features, a diagnosis of Bronchocentric Granulomatosis was made.

Follow up

   The patient was asymptomatic throughout she did not receive treatment. On follow up, after initial increase in size, the nodules started regressing and serial chest X-ray’s showed complete resolution of the lung lesions in four months. She has since been followed up in the respiratory clinic for five years and there was no radiological evidence of recurrence. Her serial spirometry during follow up was normal. She remains asymptomatic and has joined the police force leading an active lifestyle.



   Bronchocentric granulomatosis is a necrotizing granulomatous inflammation of the small to medium sized bronchi and bronchioles (1). Approximately half the patients are asthmatics and among these patients, the disease appears to be a hypersensitivity reaction to inhaled allergens particularly Aspergillus fumigatus. (2,3). In the non-asthmatic group, the causative agent is usually not identified. Similar appearances have been described in patients with Pulmonary Echinococcosis, Wegener’s Granulomatosis and Rheumatoid Arthritis (4). Occasionally, it may show histological features indistinguishable from tuberculosis.

    Asthmatic patients, who are usually in the age group 20-40 years, present with worsening wheeze, dyspnoea, cough, fever and occasionally haemoptysis. Peripheral blood may show eosinophilia and Aspergillus fumigatus is commonly grown in sputum culture. Non-asthmatic patients are often asymptomatic or may present with an acute febrile illness. Radiologically, Bronchocentric Granulomatosis can present as mass lesions, alveolar infiltrates, pneumonic consolidation or reticulo-nodular opacities (5). As this can mimic malignancy as in our case, a surgical lung biopsy may be required to rule out vasculitis or malignancy.  There are no definite diagnostic criteria and diagnosis is based on clinical, radiological and pathological correlation. Some patients may need corticosteroids for rapid clinical and radiological resolution while others recover without treatment. Surgical resections have been done to firmly establish the diagnosis given the concern about malignancy. However, when there are no alarming symptoms or signs, it may be appropriate to monitor progress or consider medical treatment.

    Bronchocentric Granulomatosis though rare is a reassuringly benign and usually self-limiting condition, which can present with alarming radiological signs. It should be considered in the asthmatic and asymptomatic patient when other sinister causes are ruled out by definitive investigations, which may include a surgical biopsy.


   Dr. Nazar Alsanjari, Pathology department, Basildon University Hospital, Basildon. For kindly providing the photomicrographs of the biopsy specimens.



1. Liebow AA. Pulmonary angiitis and granulomatosis. American Review of Respiratory Disease 1973;108:1-18.

2.  Sulavik SB. Bronchocentric granulomatosis and allergic bronchopulmonary aspergillosis. Clin Chest Med 1988;9:609-21.


3.  Koss MN, Robinson RG, Hochholzer L. Bronchocentric granulomatosis. Hum  Pathol 1981;12:632-8.

4. Bonafede RP, Benatar SR. Bronchocentric granulomatosis and rheumatoid arthritis. Br J Dis Chest 1987;81:197-201.

5. Ward S, Heyneman LE, Flint JD, Leung AN, Kazerooni EA, Miller NL. Bronchocentric granulomatosis: computed tomographic findings in five patients. Clin Radiol 2000;55:296-300.


Corresponding author:

Balamugesh Thangakunam

Speciality Doctor

Respiratory services

Basildon University Hospital

Basildon, Essex, United Kingdom

SS16 5NL

E mail:

This case was presented at the Great Cases session at the American Thoracic society meeting in New Orleans, LA on May 16, 2009. A link to the slides used in that presentation is below.

Slide Presentation